Pulmonary infection is a common occurrence in immunocompromised patients and is associated with high mortality. Immunosuppressing drugs, such as glucocorticosteroids and cyclophosphamide have been associated with specific defects in systemic immune function but little is known regarding their effects on local pulmonary host defense mechanisms. This project will evaluate drug-induced pulmonary immunopathology in an animal model of immunosuppression and based upon this information, attempts will be made to enhance pulmonary host defense during periods of peak susceptibility. Guinea pigs will receive one week courses of parenteral cortisone acetate, 100 micrograms/kg/day plus cyclophosphamide, 15 micrograms/kg/day or 30 micrograms/kg/day, Bronchoalveolar lavage fluids will then be obtained for cell enumeration differentiation and studies of the functional capabilities of cells (alveolar macrophages and lymphocytes) during immunosuppressed states. Normal animals will serve as controls. Besides cell number, an evaluation of antibacterial functions, phagocyte chemotaxis, complement synthesis by macrophages, and lymphocyte-lymphokine production will be made. Attempts to augment acute pulmonary inflammation in immuno- and myelosuppressed animals using granulocyte and monocyte transfusion therapy will be made. Likewise, efforts to augment cell-mediated immune responses in the lung with immunoadjuvants will be made. Finally, human bronchoalveolar cells, obtained from immunosuppressed patients by lung lavage, will be studied with similar techniques, in an attempt to